Brain Research最新文献

{"title":"Phenotypic plasticity: historical context, theories and DOHaD","authors":"Joaci Pereira dos Santos Júnior ,&nbsp;Osmar Henrique dos Santos Júnior ,&nbsp;Eulália Rebeca Silva-Araujo ,&nbsp;Henrique José Cavalcanti Bezerra Gouveia ,&nbsp;Diego Cabral Lacerda ,&nbsp;Diego Bulcão Visco ,&nbsp;Paula Brielle Pontes Silva ,&nbsp;Erika Vanessa Cadena-Burbano ,&nbsp;Isla Ariadny Amaral de Souza Gonzaga Paz ,&nbsp;Sandra Lopes de Souza ,&nbsp;Raul Manhães de Castro","doi":"10.1016/j.brainres.2025.149673","DOIUrl":"10.1016/j.brainres.2025.149673","url":null,"abstract":"<div><div>The Developmental Origins of Health and Disease (DOHaD) concept has emerged as an interdisciplinary framework that explores how early-life events shape long-term health and disease risk. Rooted in the Thrifty Phenotype hypothesis proposed by Barker and Hales, DOHaD builds upon centuries of philosophical and scientific thought. Central to DOHaD is the concept of phenotypic plasticity, which explains how organisms adapt their biological characteristics in response to environmental stimuli, particularly during critical developmental periods. In this context, this review aims to analyze the historical evolution of phenotypic plasticity, its theoretical foundations, and its role in health and disease. After reviewing the literature on scope, we summarize key contributions from evolutionary biology, genetics, and epigenetics, examining theories from Lamarck, Darwin, Mendel, and Waddington to contemporary perspectives in DOHaD. Understanding that early-life events can lead to adaptations which may have short-term benefits but potentially increase the likelihood of diseases in adulthood highlights the importance of targeted preventive interventions. Additionally, individual variations in response to environmental stimuli reinforce the complexity of adaptive mechanisms. Thus, understanding the intricate relationship between phenotypic plasticity, early-life exposures, and disease risk is essential for developing preventive interventions and public health strategies. The challenge remains in translating these findings into effective healthcare policies and clinical applications, ensuring improved quality of life and disease prevention across generations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149673"},"PeriodicalIF":2.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochonic acid 5, an ATP production accelerator, protects against neurological damage in ischemic stroke","authors":"Shinomi Sasaibe,&nbsp;Yukie Yoshioka,&nbsp;Yoshiki Kuse,&nbsp;Shinsuke Nakamura,&nbsp;Masamitsu Shimazawa","doi":"10.1016/j.brainres.2025.149664","DOIUrl":"10.1016/j.brainres.2025.149664","url":null,"abstract":"<div><div>Cerebral infarction is a severe condition that causes motor dysfunction and disorientation due to irreversible neuronal cell death. After an ischemic stroke, the lack of oxygen and nutrients induces cerebral neuronal damage along with mitochondrial dysfunction. Therefore, activating mitochondrial function is a promising strategy for treating ischemic stroke. This study aimed to examine whether Mitochonic acid 5 (MA-5), a compound that targets mitochondria to stimulate ATP synthesis, has protective effects against cerebral ischemia/reperfusion (I/R) injury. We first confirmed that MA-5 significantly increases ATP production after 1 h of exposure to neuron-like cells. MA-5 also increased ATP production coupled respiration in SH-SY5Y cells after the induction of OGD/R. After inducing cerebral I/R in mice via transient midbrain occlusion (t-MCAO), the administration of MA-5 reduced neurological deficits and infarct volume. In addition, MA-5 suppressed the increase in the Bax/Bcl-2 ratio, an index of mitochondria-mediated apoptosis after t-MCAO. Taken together, these results suggest that MA-5 may be a useful therapeutic agent against ischemic stroke by activating mitochondrial function.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149664"},"PeriodicalIF":2.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-channel implantable micro-magnetic stimulator for synergistic magnetic neuromodulation","authors":"Lei Dong ,&nbsp;Yenan Qi ,&nbsp;Mengying Luan ,&nbsp;Qiwen Liu ,&nbsp;Meng Wang ,&nbsp;Chunxiao Tian ,&nbsp;Yu Zheng","doi":"10.1016/j.brainres.2025.149679","DOIUrl":"10.1016/j.brainres.2025.149679","url":null,"abstract":"<div><div>Micro-magnetic stimulation (μMS) is an emerging technology in magnetic neuromodulation. However, for larger brain structures with complex neural pathways, such as deep brain neural clusters, traditional implantable single-point μMS devices are immobile and incapable of multi-regional magnetic modulation. While multi-channel μMS can effectively address this limitation, its large size, difficulty in implantation, and unclear synergistic modulation patterns restrict its application. To tackle these challenges, this study designs a 4 × 4 array micro-coil structure targeted at the deep hippocampal region of the mouse brain. Numerical simulations were performed to analyze the coupling coefficients among the micro-coils and the distribution of the electromagnetic field in the structure, indicating that, with optimized parameters, the effective magnetic stimulation threshold can be achieved. Based on this, a multi-channel μMS device was fabricated, solving key issues such as waterproofing, biocompatibility, and dual-brain-region implantation of both stimulation and recording electrodes. A multi-point synergistic magnetic stimulation protocol was developed. After determining the synergistic magnetic stimulation parameters and effective target positions through in vitro experiments, real-time monitoring of calcium signal changes in the CA1 region of the hippocampus in mice during synergistic magnetic stimulation was performed. The results demonstrate that synergistic magnetic stimulation significantly enhances synaptic plasticity and calcium signal activity. This validates the feasibility of the implantable multi-channel micro-magnetic stimulator.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149679"},"PeriodicalIF":2.7,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143924060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges and hopes for treatment of anxiety disorder in the autistic population","authors":"Tomasz Dulski ,&nbsp;Sanata Tolak ,&nbsp;Justyna Zmorzyńska","doi":"10.1016/j.brainres.2025.149675","DOIUrl":"10.1016/j.brainres.2025.149675","url":null,"abstract":"<div><div>Anxiety disorders, marked by excessive fear and worry, are particularly prevalent in autism, affecting up to 45 % of individuals with the condition. Since the 1960s, advances in neuroscience, psychology, and psychopharmacology have enhanced understanding and treatment of anxiety disorders in general population. Standardized diagnostic criteria development facilitated accurate classification of anxiety disorders. Neurobiological research identified key brain regions forming the basis of the amygdala-centred fear circuit model. Pharmacological advancements introduced selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) as safer, first-line treatments. However, these medications show limited efficacy and significant side effects in autistic individuals, highlighting the need for alternative treatments. Cognitive-behavioural therapy (CBT) has gained empirical support, helping to reduce avoidance behaviours, but modifications are often needed for autistic individuals. Emerging therapies, including Mindfulness-Based Stress Reduction for Autism Spectrum Disorder (MASSI) and virtual reality-based interventions, are being explored for individuals with more treatment-resistant anxiety. Ongoing clinical trials are assessing medications used for other psychiatric disorders to determine their efficacy in anxiety treatment for autism. Recent genetic and neuroimaging research has revealed altered brain connectivity and genetic susceptibility in anxiety, promoting the development of personalized treatments. Despite these advances, challenges remain in optimizing interventions and addressing treatment resistance, necessitating continued research and innovation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149675"},"PeriodicalIF":2.7,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota mediated regulation of vitamin B homeostasis in autism spectrum disorders","authors":"Esma Karahmet Farhat ,&nbsp;Ines Banjari ,&nbsp;Amina Džidić-Krivić ,&nbsp;Malik Ejubović ,&nbsp;Emina Karahmet Sher","doi":"10.1016/j.brainres.2025.149661","DOIUrl":"10.1016/j.brainres.2025.149661","url":null,"abstract":"<div><div>The exact cause of autism spectrum disorder (ASD) is yet unknown, although possible causes include early childhood, foetal development, gestation, delivery mode, genetics, and environmental variables. Approximately 1% of children worldwide have ASD, and this percentage is rising. The immunological, endocrine, gut microbiota and brain-gut axis quality influence the intensity of ASD symptoms. Deficits in the composition and diversity of gut microbiota are common in children with ASD, accounting for 9–90% of these illnesses, including elevated inflammatory cytokines, inflammation, leaky gut syndrome, and pathological microflora growth. Dysbiosis can be made worse by eating issues that are prevalent in ASD. B vitamins, such as cobalamin and folate, which are essential methyl donors for DNA epigenetic changes, are usually produced by a healthy gut microbiota. 50% of people with ASD have a vitamin B deficit. This work summarises research on the impact of gut microbiota on DNA methylation and B vitamin synthesis in ASD, as well as etiological variables connected to dysbiosis. Probiotics, postbiotics, and vitamin B therapies in kids with ASD should be investigated in future studies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149661"},"PeriodicalIF":2.7,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143918127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prednisolone attenuates seizure severity and neuroinflammation in a pentylenetetrazole-induced acute epilepsy model","authors":"Rafael Bremm Padilha ,&nbsp;Gabriel de Lima Rosa ,&nbsp;Edson Fernando Müller Guzzo ,&nbsp;Amanda Muliterno Domingues Lourenço de Lima ,&nbsp;Gabriela Lazzarotto ,&nbsp;Ana Carolina Sulzbach ,&nbsp;Maria Elisa Calcagnotto ,&nbsp;Adriana Simon Coitinho","doi":"10.1016/j.brainres.2025.149672","DOIUrl":"10.1016/j.brainres.2025.149672","url":null,"abstract":"<div><div>Epilepsy is a brain disorder characterized by alterations in the neuronal environment that predispose individuals to spontaneous and recurrent epileptic seizures. One of the major challenges in recent years has been the accurate diagnosis and appropriate pharmacological management of the condition. When seizures are not well controlled, individuals may develop status epilepticus, a condition with an unfavorable prognosis that requires immediate attention and treatment. Furthermore, approximately 30 % of patients are refractory to conventional treatments. In this study, we evaluated the effects of prednisolone in an acute animal model of epileptic seizures induced by pentylenetetrazole (PTZ) at doses of 1 mg/kg and 5 mg/kg. We analyzed the severity of epileptic seizures and the modulation of pro-inflammatory cytokines in treated animals. Four treatment groups were used: saline solution, diazepam (2 mg/kg), prednisolone (1 mg/kg), and prednisolone (5 mg/kg). The animals were treated, and after 30 min, PTZ (60 mg/kg) was administered. Levels of the cytokines interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured in the hippocampus and prefrontal cortex. Animals treated with prednisolone exhibited less severe epileptic seizures compared to the saline group, along with reduced levels of pro-inflammatory cytokines, particularly in the prefrontal cortex. Some animals were also assessed using EEG. Consistent with our previous studies, prednisolone demonstrated an anticonvulsant effect at doses of 1 mg/kg and 5 mg/kg in the acute PTZ-induced seizure model.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149672"},"PeriodicalIF":2.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Method for cryopreservation of brainstem pons and medulla oblongata tissue from Sprague Dawley rats for establishing primary mixed neuron-glia cell cultures","authors":"Nicole M. Nalley,&nbsp;Sophia R. Antonopoulos Raithel,&nbsp;Daniela Silva Torres,&nbsp;Paul L. Durham","doi":"10.1016/j.brainres.2025.149665","DOIUrl":"10.1016/j.brainres.2025.149665","url":null,"abstract":"<div><div>Primary cultures of brainstem tissue can be used to investigate cellular and molecular mechanisms involved in disease pathology and to identify novel therapeutic targets that modulate neuron and glial cell activities. However, preparation of primary cultures from rodent embryos or neonatal animals is labor-intensive, and it can be difficult to produce high-quality consistent cultures. To overcome these issues, cryopreservation can be used to obtain standardized, high-quality stocks of brainstem neuronal and glial cells. We present a simplified cryopreservation method for establishing primary cell cultures of pons and medulla oblongata tissue from Sprague-Dawley neonates, using a 90:10 (v/v) fetal bovine serum/dimethyl sulfoxide cell freezing medium. Cryopreserved brainstem cells stored for up to one year in liquid nitrogen exhibited similar neuronal and glial cell morphology, cell ratios, and viability when compared to fresh cultures. The expression of proteins in neurons and glial cells implicated in pain signaling and central sensitization agreed with their reported subcellular localization. Elevated intracellular calcium levels were observed in neurons and glia in response to ATP. This method for the preparation and cryopreservation of brainstem cells for establishing primary neuron-glia cultures similar to fresh preparations, is straightforward, can be utilized for biochemical, cellular, and molecular studies, increases reproducibility, requires no special equipment or reagents, saves laboratory resources including time and money, reduces the number of animals used in research, and increases flexibility in study design.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149665"},"PeriodicalIF":2.7,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143936862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GBE1 alleviates MPTP-induced PD symptoms in mice by enhancing glycolysis and oxidative phosphorylation","authors":"Hongyan Chen ,&nbsp;Hao Ding ,&nbsp;Dongya Huang ,&nbsp;Shuo Wu","doi":"10.1016/j.brainres.2025.149663","DOIUrl":"10.1016/j.brainres.2025.149663","url":null,"abstract":"<div><div>In Parkinson’s disease (PD), the disturbance of energy metabolism due to glucose metabolic reprogramming may be a critical factor contributing to neuronal degeneration and death. Glycolysis, as the core process of glucose metabolism, not only serves as a fundamental source of energy but also integrates various metabolic pathways. However, the precise role of alterations in glycolysis-related pathways in the progression of PD remains elusive. We compared and analysed datasets from human databases of patients with PD and healthy controls to identify differentially expressed genes associated with glycolysis. Using the least absolute shrinkage and selection operator regression method and multivariate logistic regression analysis, we identified glucan-branching enzyme 1 (GBE1) as the most confident glycolytic gene implicated in PD. We validated the low expression of GBE1 in 1 − methyl − 4 − phenyl − 1,2,3,6 – tetrahydropyridine (MPTP)-induced PD animal models. Stereotaxic injection-mediated overexpression of GBE1 in striatal neurons improved motor dysfunction in these animal models. In vitro experiments demonstrated that GBE1 promotes the expression of lactate dehydrogenase A (LDHA) and lactate dehydrogenase B (LDHB), enhances cellular glycolytic flux, and thereby increases the viability of PC12 cells under MPP⁺ treatment. Additionally, GBE1 alleviates mitochondrial dysfunction and restores oxidative phosphorylation in PD. In summary, by integrating machine learning and bioinformatics approaches, we identified GBE1, a glycolysis-related gene with significant implications for PD, elucidating its crucial role in glucose metabolic reprogramming and identifying potential therapeutic targets for modulating glucose metabolism in PD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1859 ","pages":"Article 149663"},"PeriodicalIF":2.7,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AMPK mediates the anti-ferroptosis effect of acupuncture in cerebral ischemia–reperfusion rats","authors":"Rong Wang ,&nbsp;Jun-feng Xu","doi":"10.1016/j.brainres.2025.149662","DOIUrl":"10.1016/j.brainres.2025.149662","url":null,"abstract":"<div><h3>Background</h3><div>Acupuncture is clinically effective in the treatment of ischemic stroke. The report suggests that energy stress inhibits ferroptosis in part through AMPK. However, whether the effect of activating AMPK is related to ferroptosis in ischemic stroke and whether acupuncture can achieve neuroprotection against ischemic brain injury through the pathway of inhibiting ferroptosis by activating AMPK has not been confirmed.</div></div><div><h3>Methods</h3><div>In this experiment, all rats were randomly divided into 4 groups: Sham group, MCAO/R group, MA (MCAO/R + acupuncture) group, and MAM (MCAO/R + acupuncture + metformin) group. The middle cerebral artery occlusion/reperfusion injury (MCAO/R) model was created by the wire embolism method, and the MA and MAM groups received acupuncture treatment with electrotherapy (1 mA, 2/15 Hz, 20 min each), while the MAM group continued to receive metformin (oral gavage 200 mg/kg) after successful modelling. Neurological deficit score and infarct volume were measured, Prussian blue staining and mitochondrial structural changes were observed, and Fe2+ and MDA levels were determined in the brain tissue of the rats. Western blot results were analyzed to determine differences in the expression of TFR1, SLC7A11, GPX4 and AMPK、p-AMPK proteins in order to explore the possible pathological processes involved in cerebral ischemia at behavioral, histological and molecular levels and the possible protective mechanisms of acupuncture.</div></div><div><h3>Results</h3><div>Acupuncture attenuated ischemia–reperfusion-induced brain damage and mitochondrial damage. Further studies showed that acupuncture reduced the levels of Fe2+, MDA and the expression of TFR1 protein and increased the expression of SLC7A11 and GPX4 protein in the diseased hippocampal region of MCAO/R rats. In addition, metformin, as an AMPK activator, significantly enhanced the protective effect of acupuncture on cerebral ischemic injury and enhanced the acupuncture-mediated reduction of Fe2+, MDA levels and TFR1 protein expression and the increase of SLC7A11 and GPX4 protein expression in the lesioned hippocampal region of MCAO/R rats.</div></div><div><h3>Conclusions</h3><div>These findings suggest that acupuncture can inhibit ferroptosis and thus exert a protective effect against ischemic brain injury, and that this mechanism may be achieved by activating AMPK. This extends the mechanism of action of acupuncture in the treatment of ischemic stroke.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149662"},"PeriodicalIF":2.7,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143901901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between Electroencephalographic microstates abnormalities and cognitive dysfunction in drug-naive MDD","authors":"Qin Qin ,&nbsp;Xinyu Liu ,&nbsp;Bin Wang ,&nbsp;Xin Wang ,&nbsp;Sixiang Liang ,&nbsp;Chao Chen ,&nbsp;Meijia Li ,&nbsp;Chuanliang Han ,&nbsp;Xixi Zhao","doi":"10.1016/j.brainres.2025.149660","DOIUrl":"10.1016/j.brainres.2025.149660","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aims to investigate the link between Electroencephalography (EEG) microstate anomalies and cognitive impairments in individuals with drug-naive Major depressive disorder (MDD).</div></div><div><h3>Methods</h3><div>We recruited 29 patients with drug-naive MDD and 30 healthy controls. The Hamilton Depression Rating Scale (HDRS-17) measured symptom severity, the MATRICS Consensus Cognitive Battery (MCCB) assessed neurocognitive function, and resting-state EEG data were collected using 64 scalp electrodes. Analysis of EEG microstates was conducted via the Microstate Analysis plugin for EEGLAB.</div></div><div><h3>Results</h3><div>MDD group had lower scores in six neurocognitive MCCB domains. For EEG microstates, four similar ones (A − D) were found in both groups. Notably, microstate C duration was lower in MDD group (t = 4.549, <em>P</em> &lt; 0.001), microstate D occurrence (t = 2.258, <em>P</em> = 0.028) and proportion (t = 3.733, <em>P</em> &lt; 0.001) were lower in MDD group. There were significant differences in all 4 microstate transition probabilities between groups. For example, A − B, B − A etc. transitions were higher in MDD, while A − C, A − D etc. were lower.<!--> <!-->The proportion of microstate D was found positively correlated with Speed of processing (SOP) score (r = 0.499, df = 26, <em>P</em> = 0.007) and Working memory (WM) score (r = 0.451, df = 26, <em>P</em> = 0.016). The Occurrence of microstate D was found positively correlated with SOP score (r = 0.383, df = 26, <em>P</em> = 0.044) and WM score (r = 0.389, df = 26, <em>P</em> = 0.041).</div></div><div><h3>Conclusions</h3><div>MDD patients show alterations in sub-second brain dynamics, characterized by a decreased proportion and occurrence of microstate D and shorter duration of microstate C, and significant shifts in microstate transition probabilities. These changes correlate with cognitive deficits across several domains, including processing speed and working memory.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1860 ","pages":"Article 149660"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143911868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}